How Brain Fat Conquers Stress Michael A. Welte  Cell  Volume 163, Issue 2, Pages 269-270 (October 2015) DOI: 10.1016/j.cell.2015.09.046 Copyright © 2015 Elsevier Inc. Terms and Conditions

Figure 1 Lipid Droplets Enable Neuroblast Proliferation in Hypoxic Conditions Left: during normal development, neuroblasts divide asymmetrically, regenerating the neuroblast and generating daughters that will give rise to neurons. Adjacent glial cells provide the stem cell niche for the neuroblasts. Right: a magnified view of the glia/neuroblast interface shows the lipid bilayers that make up the plasma membranes of the glia and neuroblast cells. Lipids containing PUFAs are shown in green; lipids damaged by peroxidation are in red. At normal oxygen levels, neuroblasts keep dividing. Under hypoxic conditions and in the absence of lipid droplets, ROS induces lipid peroxidation in membranes, which in turn gives rise to 4-HNE adducts on proteins. 4-HNE causes more ROS, resulting in an escalating feedback loop. The accumulating damage brings neuroblast proliferation to a halt. When glial lipid droplets are present, hypoxic conditions lead to a redistribution of membrane lipids (including PUFA-containing ones) to lipid droplets where they are protected from ROS-induced damage. Because membranes now contain fewer targets for lipid peroxidation, the feedback loop is dampened, and overall damage remains mild enough for neuroblasts to continue proliferating. It is not fully resolved if hypoxic remodeling lowers the relative concentration of PUFAs in the membrane (e.g., by reducing the ratio of lipids to proteins) or if total membrane surface shrinks. Cell 2015 163, 269-270DOI: (10.1016/j.cell.2015.09.046) Copyright © 2015 Elsevier Inc. Terms and Conditions